Androgenetic alopecia is the most common type of hair loss, which was once widely known as “seborrheic alopecia”, and was also called “toplessness”, “early baldness”, “male pattern baldness”, “androgenic baldness” and “genetic alopecia”. “Male pattern baldness”, “androgenic baldness”, “genetic alopecia”, etc., are actually all referring to the same phenomenon. I did not call it a disease because in a sense it is a characteristic expression of the individual, just as some men have particularly thick beards while others have almost none, and some have thick human hair while others have little visible. Because of the aesthetic relationship, society and individuals cannot accept this manifestation, which is why so many people go around seeking treatment. So, why has the professional name “seborrheic alopecia” been abandoned in favor of “androgenic alopecia”? This also starts from the pathogenesis. What is abnormal is that the hair follicles in the hair loss area are sensitive to androgens, and the hair follicles become smaller and smaller under the action of the normal level of androgens, and the corresponding hairs also become small and cannot grow. In addition to the androgen sensitivity of the hair follicles, the sebaceous glands are also androgen sensitive, producing large amounts of sebum, making the skin and hair greasy and prone to dandruff. It is the fact that the two often appear together that makes people mistakenly believe that the change in hair is caused by excessive oil accumulation. With the development of modern medicine, it is clear that hair loss and oiliness are two juxtaposed results rather than a causal relationship, so oil control alone cannot play a role in preventing hair loss and growth. However, if the scalp is very oily, minor inflammatory reactions such as seborrheic dermatitis or folliculitis persist for a long time and have an effect on hair growth, so it cannot be ignored. Why are some people’s hair follicles sensitive to androgens? This has something to do with genetics. Hair follicles in sensitive areas have more androgen receptors and 5a-reductase activity than those in non-sensitive areas or non-hair loss. These differences are determined by genes, which originate from the father and mother, in addition to which some genes are born altered when new individuals are created, so that the hair condition of the parents determines the level of risk of hair loss in their children, but the children’s hair loss is different, either heavier or lighter than their parents. In addition to androgens and genes that play a decisive role in the development of this hair loss, there are other factors that have a more or less significant impact on the development of hair loss, mainly heavy smoking and irregular lifestyle tend to exacerbate hair loss, while diet has no evidence that it can influence hair loss. Regarding treatment, because of the limitations in understanding the pathogenesis, only two drugs have been widely proven safe and effective. One is the oral drug 1 mg finasteride, one tablet per day, for adult males; the other is a topical 1-5% minoxidil preparation, which requires twice daily use for both men and women. The two may work better together, but the monthly cost is correspondingly higher. It is important to note that women of childbearing age are not allowed to take finasteride orally to prevent abnormal development of the extra-urinary genital system of the fetus after pregnancy. To date, no herbal medicine has been proven to treat androgenic alopecia, and it is not certain how much of a therapeutic effect cystine and vitamin B can have. Therefore, I prescribe very simple medications for treatment, finasteride tablets and/or minoxidil preparations, and supplemental anti-inflammatory and de-oiling medications depending on the local condition of the scalp.